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respiratory infections

Monday 16 March 2009

Some 10,000 microorganisms, including viruses, bacteria, and fungi, are inhaled daily by every city inhabitant. The distance these microorganisms travel into the respiratory system is inversely proportional to their size.

Large microbes are trapped in the mucociliary blanket that lines the nose and the upper respiratory tract. Microorganisms are trapped in the mucus secreted by goblet cells and are then transported by ciliary action to the back of the throat, where they are swallowed and cleared.

Organisms smaller than 5 μm travel directly to the alveoli, where they are phagocytosed by alveolar macrophages or by neutrophils recruited to the lung by cytokines.

Damage to the mucociliary defense results from repeated insults in smokers and patients with cystic fibrosis, while acute injury occurs in intubated patients and in those who aspirate gastric acid.

Successful respiratory microbes evade the mucociliary defenses in part by attaching to epithelial cells in the lower respiratory tract and pharynx. For example, influenza viruses possess hemagglutinin proteins that project from the surface of the virus and bind to sialic acid on the surface of epithelial cells.

This attachment induces the host cell to engulf the virus, leading to viral entry and replication within the host cell. However, sialic acid binding prevents newly synthesized viruses from leaving the host cell. Influenza viruses have another cell surface protein, neuraminidase, which cleaves sialic acid and allows virus to release from the host cell.

Neuraminidase also lowers the viscosity of mucus and facilitates viral transit within the respiratory tract. Interestingly, some anti-influenza drugs are sialic acid analogs that inhibit neuraminidase and prevent viral release from host cells.

Certain respiratory bacterial pathogens can impair ciliary activity. For instance, Haemophilus influenzae and Bordetella pertussis elaborate toxins that paralyze mucosal cilia; Pseudomonas aeruginosa, a cause of severe respiratory infection in persons with cystic fibrosis, and Mycoplasma pneumoniae produce ciliostatic substances.

Some bacteria such as Streptococcus pneumoniae or Staphylococcus species lack specific adherence factors and often gain access after viral infection causes loss of ciliated epithelium, making individuals who have had viral respiratory infection more susceptible to secondary bacterial respiratory infection. Mycobacterium tuberculosis, in contrast, gains its foothold in normal alveoli because it is able to escape phagocytic killing by macrophages.

Growth requirements for microorganisms can determine their site of infection in the respiratory tract. For example, rhinoviruses, which cause the common cold, grow optimally at 33°C, the temperature of the nasal mucosa, but grow poorly at 37°C, the temperature of the lower respiratory tract.

Finally, opportunistic fungi infect the lungs when cellular immunity is depressed or when leukocytes are reduced in number (e.g., P. jiroveci [carinii] in AIDS patients and Aspergillus species in chemotherapy patients).